There is universal agreement that only a fraction of the amount consumed during a meal is absorbed from the digestive system before the meal is terminated and that peripheral sensory systems, therefore, play a critical role in short-term satiety and in the control of meal size. However, considerable controversy surrounds the issue of the identity and location of the peripheral receptors from which satiety-relevant feedback originates. the debate is marked by the advocacy of single-organ models of satiety (e.g., "the stomach signals satiety") despite good evidence that receptors at several locations can provide complementary or redundant information about what has been ingested during the meal (volume, nutrient content, calories, etc.). As a result, almost no data speak to the integration of intake-inhibitory signals when feedback from oral, gastric and post-gastric sources are concurrently available. This is a serious omission for clinical approaches to feeding disorders and for neural investigations into substrates that modulate ingestive behavior as a function of physiological and metabolic variables. Experiments proposed will address these issues. The present experiments will provide a systematic analysis, in the rat, of the relative contributions of oral, gastric and post-gastric signals to terminating bouts of glucose ingestion initiated under controlled laboratory conditions. to determine the gastric versus post-gastric distribution of ingested glucose, measurement of the cumulative intake curve will be coordinated with what will be the first systematic measurements of gastric emptying during ingestion. It will thereby be possible to quantify the stimulatory effects of experimental manipulations (stimulus concentration, stimulus delivery rate, gastric infusions of glucose delivered at different rates in parallel with oral ingestion) designed to systematically bias the rate of glucose accumulation within the stomach relative to the rate at which glucose empties from the stomach. Their behavior impact will be evaluated in terms of (1) changes in meal size and meal duration, and (2) the amount of glucose within and beyond the stomach when meals are terminated. these experiments will lead to the identification of peripheral sources of satiety-relevant feedback and to an operational model for the integrative mechanisms that underlie short-term satiety under normal conditions when oral, gastric and postgastric receptors are stimulated concurrently.